Protective effect of cyclosporine on inflammatory injury of renal tubular epithelial cells

OBJECTIVE: This study aims to explore the protective effect of cyclosporine on inflammation-induced renal tubular epithelial cells and its potential mechanism. MATERIALS AND METHODS: Human kidney-2 (HK-2) cells were induced by transforming growth factor-beta (TGF-beta) for constructing an inflammatory injury model. Cells were then treated with different concentrations of cyclosporine for further investigating the biological functions. Cell viability was detected via cell counting kit-8 assay (CCK-8). The cytotoxicity was detected via lactate dehydrogenase (LDH) release assay. Expression levels of cell damage factors and mammalian target of rapamycin (mTOR) pathway-related genes were detected via polymerase chain reaction (PCR), immunofluorescence and Western blotting, respectively. RESULTS: TGF-beta inhibited the viability of HK2 cells, increased expressions of tumor necrosis factor-a (TNF-a), interleukin-1 beta (IL-1 beta) and apoptosis-related genes. Cyclosporine treatment greatly reversed the cell damage on HK-2 cells induced by TGF-beta. Expression levels of mTOR pathway-related genes were downregulated after cyclosporine treatment. CONCLUSIONS: Cyclosporine protects HK-2 cells from inflammatory injury via regulating mTOR pathway.